Absence of stretch reflex gain enhancement in voluntarily activated spastic muscle

doi:10.1016/0014-4886(87)90245-7

Experimental Neurology

Volume 98, Issue 2, November 1987, Pages 317-335

https://doi.org/10.1016/0014-4886(87)90245-7 Get rights and content

Abstract

Static and dynamic stiffnesses of voluntarily activated elbow muscles were compared in spastic and contralateral arms of 15 subjects with spastic hemiparesis. Stiffnesses were estimated from the positional deflections induced by applying load perturbations to each forearm. In $1115$ subjects (73%), stiffnesses were comparable on the two sides. In the remaining $415$ subjects (27%), stiffnesses were consistently greater on the spastic side, however, EMG recordings from these spastic muscles were of much smaller amplitude than those of the contralateral muscles, indicating that this increase was probably caused by changes in the mechanical properties of elbow muscles, rather than by stretch reflex enhancement. We conclude that for voluntarily activated muscles of spastic hemiparetic subjects, reflex stiffness (and presumably stretch reflex gain), of spastic and contralateral limbs is not significantly different. These findings impose important constraints upon theories attempting to explain spastic hypertonia, and they also provide guidelines for clinical quantification of spasticity.

References (28)

V. Dietz et al.
Normal and impaired regulation of muscle stiffness in gait: a new hypothesis about muscle hypertonia
Exp. Neurol.
(1983)
D.G. Asatryan et al.
Functional tuning of nervous system with control of movement or maintenance of a steady posture. I. Mechanographic analysis of the work of the joint on execution of a postural task
Biofizika
(1965)
D. Bourbonnais et al.
Patterns of muscle activity during isometric contraction in spastic hemiparesis
Soc. Neurosci. Abstr.
(1986)
W. Berger et al.
Tension development and muscle activation in the leg during gait in spastic hemiparesis: independence of muscle hypertonia and exaggerated stretch reflexes
J. Neurol. Neurosurg. Psychiatry
(1984)
B. Bishop
Spasticity: its physiology and management
Phys. Ther.
(1977)
D. Burke
A reassessment of the muscle spindle contribution to muscle tone in normal and spastic man
P.E. Crago et al.
Regulatory actions of human stretch reflex
J. Neurophysiol.
(1976)
P.J. Delwaide
Étude expérimentale de l'hyperréflexie tendineuse en clinique neurologique
P. Dietrichson et al.
Clinical method for electrical recording of the mechanically and electrically elicited ankle reflex
Acta Neurol. Scand.
(1971)
V. Dietz et al.
Electrophysiological studies of gait in spasticity and rigidity: evidence that altered mechanical properties of muscle contribute to hypertonia
Brain
(1981)

W.J. Dixon et al.

C.C.A.M. Gielen et al.

Viscoelastic properties of the wrist motor servo in man

Ann. Biomed. Eng.

(1984)

G.R. Gottlieb et al.

Sinusoidal oscillation of the ankle as a means of evaluating the spastic patient

J. Neurol. Neurosurg. Psychiatry

(1978)

R. Herman

Reflex and rheologic properties of the spastic gastrocnemius soleus muscle group

Arch. Phys. Med.

(1968)

Cited by (100)

Modification of Spastic Stretch Reflexes at the Elbow by Flexion Synergy Expression in Individuals With Chronic Hemiparetic Stroke
2018, Archives of Physical Medicine and Rehabilitation
To systematically characterize the effect of flexion synergy expression on the manifestation of elbow flexor stretch reflexes poststroke, and to relate these findings to elbow flexor stretch reflexes in individuals without neurologic injury.
Controlled cohort study.
Academic medical center.
Participants (N=20) included individuals with chronic hemiparetic stroke (n=10) and a convenience sample of individuals without neurologic or musculoskeletal injury (n=10).
Participants with stroke were interfaced with a robotic device that precisely manipulated flexion synergy expression (by regulating shoulder abduction loading) while delivering controlled elbow extension perturbations over a wide range of velocities. This device was also used to elicit elbow flexor stretch reflexes during volitional elbow flexor activation, both in the cohort of individuals with stroke and in a control cohort. In both cases, the amplitude of volitional elbow flexor preactivation was matched to that generated involuntarily during flexion synergy expression.
The amplitude of short- and long-latency stretch reflexes in the biceps brachii, assessed by electromyography, and expressed as a function of background muscle activation and stretch velocity.
Increased shoulder abduction loading potentiated elbow flexor stretch reflexes via flexion synergy expression in the paretic arm. Compared with stretch reflexes in individuals without neurologic injury, paretic reflexes were larger at rest but were approximately equal to control muscles at matched levels of preactivation.
Because flexion synergy expression modifies stretch reflexes in involved muscles, interventions that reduce flexion synergy expression may confer the added benefit of reducing spasticity during functional use of the arm.
Contributions of motoneuron hyperexcitability to clinical spasticity in hemispheric stroke survivors
2015, Clinical Neurophysiology
Muscle spasticity is one of the major impairments that limits recovery in hemispheric stroke survivors. One potential contributing mechanism is hyperexcitability of motoneurons. Previously, the response latency of the surface electromyogram (EMG) record evoked by joint rotation has been used to characterize motoneuron excitability. Given the limitations of this method, the objective of the current study was to reexamine the excitability of motoneurons in chronic stroke survivors by estimating reflex latency using single motor unit discharge.
We quantified the excitability of spastic motoneurons using the response latency of a single motor unit discharge elicited by a position controlled tap on the biceps brachii tendon. We applied tendon taps of different amplitudes on the biceps tendons of both arms of the stroke survivors. Unitary reflex responses were recorded using intramuscular EMG recordings.
Our results showed that the latency of unitary discharge was systematically shorter in the spastic muscle compared with the contralateral muscle, and this effect was consistent across multiple tap amplitudes.
This method allowed us to quantify latencies more accurately, potentially enabling a more rigorous analysis of contributing mechanisms.
The findings provide evidence supporting a contribution of hyperexcitable motoneurons to muscle spasticity.
Characterizations of reflex and nonreflex changes in spastic multiple sclerosis
2014, Journal of Neuroscience Methods
Spasticity, an increased resistance of a limb to movement, is associated with functional limitations and a major source of disability in neurological disorders, including multiple sclerosis (MS) and stroke. Despite the clinical significance of spasticity in brain and spinal cord injuries, it is often not clear whether the spasticity is due to reflex or non-reflex changes.
Reflex and nonreflex properties of the human knee joint were studied in eight MS patients with spasticity and ten healthy subjects. A digitally controlled joint driving device was used to apply small-amplitude, and band-limited white-noise perturbations to the knee to manifest the reflex and nonreflex properties. The subjects were asked to maintain a steady level of background muscle torque during the perturbation. A nonlinear delay differential equation model was used to characterize the reflex and intrinsic properties of the knee in terms of phasic stretch reflex gain, tonic stretch reflex gain, joint elastic stiffness, and coefficient of viscosity.
It was found that joint coefficient of viscosity and tonic stretch reflex gain of the spastic MS patients were significantly lower than those of normal controls. On the other hand, spastic MS patients showed higher phasic stretch reflex gains than normal controls and a trend of increased joint stiffness.
Simultaneous characterizations of changes in tonic and phasic reflexes and nonreflex changes in joint elastic stiffness and viscosity in neurological disorders may help us gain insight into mechanisms underlying spasticity and develop impairment-specific treatment.
Gait disorders
2013, Handbook of Clinical Neurology
Citation Excerpt :
During gait there is no visible influence of short-latency reflex potentials on the tension developed by the triceps surae. A similar discrepancy between the resistance to stretch and the level of EMG activity has been described for flexor muscles of the upper limb in spastic patients (Lee et al., 1987; Powers et al., 1988). Spastic muscle tone during functional movements cannot be explained by an increased activity of motoneurons, but instead by a transformation of motor units such that a higher triceps surae tension to EMG activity relationship occurs during the stretching period in the stance phase of gait (Dietz and Sinkjaer, 2007; Fig. 12.4).
This chapter deals with the neuronal mechanisms underlying impaired gait. The aim is, first, a better understanding of the underlying pathophysiology and, second, the selection of an adequate treatment. One of the first symptoms of a lesion within the central motor system perceived by patients is a movement disorder, which is most characteristic during locomotion, e.g. in patients suffering spasticity after stroke or a spinal cord injury or Parkinson disease. By the recording and analysis of electrophysiological and biomechanical signals during a movement, the significance of impaired reflex behavior or muscle tone and its contribution to the movement disorder can reliably be assessed. Adequate treatment should not be restricted to the correction of an isolated clinical sign but should be based on the mechanisms underlying the movement disorder that impairs the patient. Therapy should be directed toward functional training, which takes advantage of the plasticity of the nervous system. In the future a combination of repair and functional training will further improve the mobility of disabled patients.
Spasticity measurement based on tonic stretch reflex threshold in stroke using a portable device
2008, Clinical Neurophysiology
We investigated intra- and inter-evaluator reliability to quantify spasticity based on the tonic stretch reflex threshold (TSRT) and the correlation between TSRT and resistance to stretch.
Spasticity was evaluated in 20 subjects with chronic stroke-related spasticity using a portable device and the Modified Ashworth Scale (MAS). Evaluations were done on 2 days, by three evaluators. Biceps brachii EMG signals and elbow displacement were recorded during 20 elbow stretches applied at different velocities for each evaluation. Velocity-dependent dynamic stretch reflex thresholds (angle where EMG signal increased in the biceps for a given velocity of stretch) were recorded. These values were used to compute TSRT (excitability of motoneurons at 0°/s). Spasticity was also measured with MAS.
Reliability was moderately good for subjects with moderate to high spasticity (intra-evaluator: 0.46–0.68, and inter-evaluator: 0.53–0.68). The TSRT measure of spasticity did not correlate with resistance to stretch (MAS).
TSRT may be a more representative measure for subjects with moderate to high spasticity. Further improvements are suggested for the portable device in order to quantify all the levels of spasticity.
TSRT may be an alternative clinical measure to current clinical scales.
Implementation of Impairment-Based Neurorehabilitation Devices and Technologies Following Brain Injury
2022, Neurorehabilitation Technology, Third Edition

View all citing articles on Scopus

²: W.A.L.'s current affiliation is Programs in Physical Therapy, Northwestern University Medical School.

¹: The authors are grateful to the staff of the Rehabilitation Institute of Chicago for referring their patients. Special thanks are offered to Dr. W. A. Adair, Dr. P. Kaplan, Dr. M. Kim, Dr. S. Lal, Dr. W. Nimmer, Dr. V. Sahgal, and Dr. Y. Wu. The research described was supported by NIH grant NS 19331, NIHR grant G008300079 (W.Z.R.) and by the Coleman, Hearst, J. M. Joyce, Regenstein, and Searle Foundations.

View full text

Absence of stretch reflex gain enhancement in voluntarily activated spastic muscle

Abstract

Exp. Neurol.

Functional tuning of nervous system with control of movement or maintenance of a steady posture. I. Mechanographic analysis of the work of the joint on execution of a postural task

Biofizika

Patterns of muscle activity during isometric contraction in spastic hemiparesis

Soc. Neurosci. Abstr.

Tension development and muscle activation in the leg during gait in spastic hemiparesis: independence of muscle hypertonia and exaggerated stretch reflexes

J. Neurol. Neurosurg. Psychiatry

Spasticity: its physiology and management

Phys. Ther.

A reassessment of the muscle spindle contribution to muscle tone in normal and spastic man

Regulatory actions of human stretch reflex

J. Neurophysiol.

Étude expérimentale de l'hyperréflexie tendineuse en clinique neurologique

Clinical method for electrical recording of the mechanically and electrically elicited ankle reflex

Acta Neurol. Scand.

Electrophysiological studies of gait in spasticity and rigidity: evidence that altered mechanical properties of muscle contribute to hypertonia

Brain

Viscoelastic properties of the wrist motor servo in man

Ann. Biomed. Eng.

Sinusoidal oscillation of the ankle as a means of evaluating the spastic patient

J. Neurol. Neurosurg. Psychiatry

Reflex and rheologic properties of the spastic gastrocnemius soleus muscle group

Arch. Phys. Med.